Immune Responses to the Hepatitis C Virus

2014 ◽  
pp. 476-486
Author(s):  
David G. Bowen ◽  
Patrick Bertolino
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses

Enhanced immune responses, PI3K/AKT and JAK/STAT signaling pathways following hepatitis C virus eradication by direct-acting antiviral therapy among Egyptian patients: a case control study

2021 ◽  
Author(s):  
Haidi Karam-Allah Ramadan ◽  
Gamal Badr ◽  
Nancy K Ramadan ◽  
Aml Sayed
Keyword(s):  
Immune Response ◽  
Liver Cirrhosis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Signaling Pathways ◽  
Liver Diseases ◽  
Stat Signaling ◽  
Chronic Hcv ◽  
Direct Acting

Abstract The use of direct-acting antivirals (DAAs) therapy for the treatment of hepatitis C virus (HCV) results in a high sustained virological response (SVR) and subsequently alters liver immunologic environment. However, hepatocellular carcinoma (HCC) may occur after DAAs treatment. We aimed to clarify changes of immune responses, PI3K/AKT and JAK/STAT signaling pathways in HCV-induced liver diseases and HCC following DAAs treatment. Four cohorts are classified as chronic HCV patients, HCV-related cirrhosis without HCC, HCV-related cirrhosis and HCC, and healthy control group. The patient groups were further divided into treated or untreated with DAAs with SVR12. Increased percentages of CD3, CD8 and CD4, decreased CD4/FoxP3/CD25, CD8/PD-1 and CD19/PDL-1 were found in DAAs-treated patients in the three HCV groups. Following DAAs therapy, the levels of ROS, IL-1β, IL-6, IL-8 and TNF-α were significantly decreased in the three HCV groups. Treated HCV patients showed up regulation of p-AKT and p-STAT5 and down regulation of p-STAT3, HIF-1α and COX-2. In conclusion, DAAs enhance the immune response in chronic HCV and liver cirrhosis, hence our study is the first to show change in PI3K/AKT and JAK/STAT signaling pathways in different HCV-induced liver diseases after DAAs. In chronic HCV, DAAs have better impact on the immune response while in liver cirrhosis not all immune changes were prominent.

scholarly journals Multiple Fixed Drug Eruption Mimicking Parapsoriasis en Plaque in a Patient with Hepatitis C Virus Infection

2020 ◽  
Vol 12 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Michie Katsuta ◽  
Akihiko Asahina ◽  
Tetsuo Shiohara
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Drug Eruption ◽  
Hcv Rna ◽  
Fixed Drug Eruption ◽  
Cutaneous Manifestations ◽  
Fixed Drug ◽  
Per Se ◽  
Multiple Drugs

Although hepatitis C virus (HCV) infection is often associated with extrahepatic cutaneous manifestations such as lichen planus, it is unclear whether HCV per se or HCV-specific immune responses play a pathophysiological role in the development of HCV-related cutaneous diseases. We recently treated a patient who developed parapsoriasis en plaque-like lesions after ingestion of various drugs. She showed hypersensitivity to multiple drugs after interferon therapy. Her clinical course was complicated by flares of parapsoriasis-like lesions which returned at precisely the same sites. The flares had begun within hours of ingesting nicardipine hydrochloride, amlodipine besilate, candesartan cilexetil and atenolol for the first time despite showing a low level of HCV RNA. Interestingly, the flares gradually subsided during continued treatment with these drugs while her HCV RNA level paradoxically increased: thus, there was an inverse correlation between flares and HCV RNA level. The eruptions were eventually diagnosed as fixed drug eruption, although the clinical manifestations mimicked parapsoriasis en plaque. Our results suggest that multiple drug hypersensitivity could be induced by antiviral immune responses that are cross-reactive to multiple drugs, but not by HCV per se.

scholarly journals Hepatitis C Virus Induces Toll-Like Receptor 4 Expression, Leading to Enhanced Production of Beta Interferon and Interleukin-6

2006 ◽  
Vol 80 (2) ◽  
pp. 866-874 ◽  
Author(s):  
Keigo Machida ◽  
Kevin T. H. Cheng ◽  
Vicky M.-H. Sung ◽  
Alexandra M. Levine ◽  
Steven Foung ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cells ◽  
Immune Responses ◽  
Interleukin 6 ◽  
Innate Immune ◽  
Hcv Infection ◽  
Innate Immune Responses ◽  
Altered Expression ◽  
Beta Interferon

ABSTRACT Hepatitis C virus (HCV) induces inflammatory signals, leading to hepatitis, hepatocellular carcinomas, and lymphomas. The mechanism of HCV involvement in the host's innate immune responses has not been well characterized. In this study, we analyzed expression and regulation of the entire panel of toll-like receptors (TLRs) in human B cells following HCV infection in vitro. Among all of the TLRs (TLRs 1 to 10) examined, only TLR4 showed an altered expression (a three- to sevenfold up-regulation) after HCV infection. Peripheral blood mononuclear cells from HCV-infected individuals also showed a higher expression level of TLR4 compared with those of healthy individuals. HCV infection significantly increased beta interferon (IFN-β) and interleukin-6 (IL-6) secretion from B cells, particularly after lipopolysaccharide stimulation. The increased IFN-β and IL-6 production was mediated by TLR4 induction, since the introduction of the small interfering RNA against TLR4 specifically inhibited the HCV-induced cytokine production. Among all of the viral proteins, only NS5A caused TLR4 induction in hepatocytes and B cells. NS5A specifically activated the promoter of the TLR4 gene in both hepatocytes and B cells. In conclusion, HCV infection directly induces TLR4 expression and thereby activates B cells, which may contribute to the host's innate immune responses.

MicroRNA-155 controls Toll-like receptor 3- and hepatitis C virus-induced immune responses in the liver

2013 ◽  
Vol 21 (2) ◽  
pp. 99-110 ◽  
Author(s):  
M. Jiang ◽  
R. Broering ◽  
M. Trippler ◽  
J. Wu ◽  
E. Zhang ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Toll Like Receptor

scholarly journals Correction for Yi et al., “Hepatitis C Virus NS4B Can Suppress STING Accumulation To Evade Innate Immune Responses”

2018 ◽  
Vol 92 (2) ◽  
Author(s):  
Guanghui Yi ◽  
Yahong Wen ◽  
Chang Shu ◽  
Qingxia Han ◽  
Kouacou V. Konan ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses

Canola oilseed‐ and Escherichia coli‐ derived hepatitis C virus (HCV) core proteins adjuvanted with oil bodies, induced robust Th1‐oriented immune responses in immunized mice

Apmis ◽  
2020 ◽  
Vol 128 (11) ◽  
pp. 593-602
Author(s):  
Sara Mohammadzadeh ◽  
Farzin Roohvand ◽  
Parastoo Ehsani ◽  
Ali Hatef Salmanian ◽  
Soheila Ajdary
Keyword(s):  
Escherichia Coli ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Oil Bodies ◽  
Core Proteins

scholarly journals Alphavirus-based hepatitis C virus therapeutic vaccines: can universal helper epitopes enhance HCV-specific cytotoxic T lymphocyte responses?

2019 ◽  
Vol 7 ◽  
pp. 251513551987467
Author(s):  
Georgia Koutsoumpli ◽  
Peng Peng Ip ◽  
Ilona Schepel ◽  
Baukje Nynke Hoogeboom ◽  
Annemarie Boerma ◽  
...  
Keyword(s):  
T Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
T Cell ◽  
Immune Responses ◽  
Semliki Forest Virus ◽  
Intracellular Cytokine Staining ◽  
Target Antigen ◽  
Optimal Dosage ◽  
Therapeutic Vaccines

Background: Antigen-specific T cell immune responses play a pivotal role in resolving acute and chronic hepatitis C virus (HCV) infections. Currently, no prophylactic or therapeutic vaccines against HCV are available. We previously demonstrated the preclinical potency of therapeutic HCV vaccines based on recombinant Semliki Forest virus (SFV) replicon particles. However, clinical trials do not always meet the high expectations of preclinical studies, thus, optimization of vaccine strategies is crucial. In efforts to further increase the frequency of HCV-specific immune responses in the candidate SFV-based vaccines, the authors assessed whether inclusion of three strong, so-called universal helper T cell epitopes, and an endoplasmic reticulum localization, and retention signal (collectively termed sigHELP-KDEL cassette) could enhance HCV-specific immune responses. Methods: We included the sigHELP-KDEL cassette in two of the candidate SFV-based HCV vaccines, targeting NS3/4A and NS5A/B proteins. We characterized the new constructs in vitro for the expression and stability of the transgene-encoded proteins. Their immune efficacy with respect to HCV-specific immune responses in vivo was compared with the parental SFV vaccine expressing the corresponding HCV antigen. Further characterization of the functionality of the HCV-specific CD8+ T cells was assessed by surface and intracellular cytokine staining and flow cytometry analysis. Results: Moderate, but significantly, enhanced frequencies of antigen-specific immune responses were achieved upon lower/suboptimal dosage immunization. In optimal dosage immunization, the inclusion of the cassette did not further increase the frequencies of HCV-specific CD8+ T cells when compared with the parental vaccines and the frequencies of effector and memory populations were identical. Conclusion: We hypothesize that the additional effect of the sigHELP-KDEL cassette in SFV-based vaccines depends on the immunogenicity, nature, and stability of the target antigen expressed by the vaccine.

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